The most common diagnosis in all of the cholestatic groups was primary biliary cirrhosis; though some patients had primary sclerosing cholangitis, progressive familial intrahepatic cholestasis, benign recurrent intrahepatic cholestasis or other liver disorders.

Key findings:

Serum autotaxin is increased in pruritic cholestatic liver patients but not in other forms of pruritus. In addition, autotaxin is normal in cholestatic patients without pruritus.

The level of autotaxin correlates closely with the effectiveness of the treatment as gauged by itch intensity

The reasons for pruritus in cholestasis have not been clear. Several theories have been advanced regarding pathogenesis. Specifically, retained bile acids and increased opiate activity have been thought to play a role. More recently, lysophosphatidic acid (LPA) levels have been noted to be elevated in the serum of patients with cholestatic itch. Injection of LPA into mice results in scratching activity. LPA activity is a consequence of autotaxin.

Other important points:

Rifampicin has been shown to reduce autotaxin levels in vivo.

MARS and nasobiliary drainage do not directly drain autotaxin; their effects on autotaxin must result by eliminating another factor which stimulates autotaxin production.

Autotaxin is likely to be a useful objective biological marker for pruritus and to evaluate potential novel treatments.

Autotaxin elevation can occur in other noncholestatic inflammatory disease in which pruritus is not a feature; thus, the reasons for pruritus are likely multifactorial and not due to a simple causal role for autotaxin.